1. Field of the Invention
This invention relates broadly to methods, devices and systems for prevention, diagnosis, and treatment of medical conditions. More particularly, this invention relates to methods, devices and systems for prevention of sudden infant death syndrome (SIDS) and for the diagnosis and treatment of infants predisposed to SIDS.
2. State of the Art
Sudden infant death syndrome (SIDS) is any sudden and unexplained death of an apparently healthy infant aged one month to one year. SIDS is responsible for roughly 0.05%, or 50 deaths per 100,000 births in the United States. It is responsible for far fewer deaths than congenital disorders and disorders related to short gestation, though it is the leading cause of death in infants that have appeared healthy after one month of age.
Very little has been known about the possible causes of SIDS, and there has been no reliable or proven method for prevention. Although studies have identified risk factors for SIDS, such as the prone sleeping position, presence of an upper respiratory infection, exposure to cigarette smoke, over-wrapping and over warming in the winter months, there has been little understanding of the syndrome's biological cause or causes.
One recent study attributes SIDS death to abnormalities in the part of the brain that helps control functions like breathing, blood pressure and arousal. Patterson et al., Multiple Serotonergic Brainstem Abnormalities in Sudden Infant Death Syndrome, JAMA, 296: 2124-2132 (2006). In this study, researchers examined the brains of 31 babies who had died of SIDS and 10 who had died from other causes. The study found that babies that died from SIDS had abnormalities in the brain stem which appeared to affect the ability to use and recycle serotonin. Serotonin levels are responsible for regulating mood as well as vital body functions. According to the National Institutes of Health, the new finding is the strongest evidence to date suggesting that innate differences in a specific part of the brain may place some at increased risk of dying from SIDS. A key point is that these results do not indicate how the brain differences that precipitate SIDS were incurred (whether, e.g., genetic disorder, disease), how to prevent SIDS, or how to treat a high risk infant so as to reduce or prevent infant mortality from those infants predisposed to SIDS. Additionally, this explanation does not take into account abnormalities of function found in other regions (such as to hearing) or explain why SIDS infants do not die in the first three weeks of life.